Implantable medical devices (IMD) are well known in the art. The IMD may take the form of implantable defibrillators or cardioverters which treat accelerated rhythms of the heart such as fibrillation. The IMD may also take the form of implantable pacemakers which maintain the heart rate above a prescribed limit, such as, for example, to treat a bradycardia. Implantable medical devices may also incorporate more than one of a pacemaker, a cardioverter and a defibrillator. Defibrillators may include “shock only” functionality or, in addition to shocking functionality, a defibrillator may be capable of providing cardiac resynchronization therapy (CRT) functionality. Shock only devices and CRT devices are typically coupled to different lead configurations. As a further example, the IMD may be an implantable monitoring device, such as the Confirm™ device offered by St. Jude Medical.
An IMD is comprised of three major components. One component, at least in stimulation type IMDs, is a pulse generator which generates the stimulation pulses and includes the electronic circuitry and the power cell or battery. The second component, at least in stimulation type IMDs, is the lead, or leads, which electrically couple the IMD to the heart. IMDs deliver stimulation pulses to the heart to cause the stimulated heart chamber to contract when the patient's own intrinsic rhythm fails. The third component is a sensor and detection module that monitors a heart for cardiac signals and analyzes the cardiac signals to identify normal sinus rhythm, arrhythmias and the like. To this end, IMDs include sensing circuits that sense cardiac activity for the detection of intrinsic cardiac events such as intrinsic atrial events (P-waves) and intrinsic ventricular events (R-waves). By monitoring P-waves and/or R-waves, the IMD circuits are able to determine the intrinsic rhythm of the heart and provide stimulation pulses that force atrial and/or ventricular depolarizations at appropriate times in the cardiac cycle when required to help stabilize the electrical rhythm of the heart.
IMDs detect various arrhythmias such as atrial fibrillation (AF), atrial flutter (A-flutter), and atrial tachycardia (AT) (hereafter collectively atrial arrhythmias). Arrhythmias are detected based on one or more of ventricular rate, rate stability, and the morphology of the cardiac signal. However, conventional algorithms for detecting arrhythmias experience certain limitations. For example, conventional AF detection algorithms that are based on rate stability may become confounded when an atrial tachyarrhythmia drives a ventricle at a high, but very stable rate. When a patient experiences atrial tachyarrhythmia having a stable rate, the AF detection algorithm may classify the events merely as high rate normal sinus events. Thus, the AF detection algorithm may not declare the events to be pathologic (non-physiologic) and may not deliver a therapy. Further, conventional algorithms may not correctly classify atrial fibrillation that exhibits rate dependent changes in the QRS complex. When a patient experiences atrial tachyarrhythmia having rate dependent changes in the QRS complex, the morphology detection algorithm may classify the events merely as physiologic events and thus, may not declare the events to be pathologic.
At least certain limitations of conventional detection algorithms extend, in part, from the fact that the algorithms analyze intra-cardiac electrogram (IEGM) signals from various combinations of electrodes within and surrounding the heart. IEGM signals are a direct indicator of the electrical activity within the tissue of the heart. While heart tissue electrical activity is a good indicator of heart behavior, the electrical activity is not a direct indicator of the resultant actual “mechanical” output of the heart. The mechanical output of the heart constitutes the actual cardiac output (CO) of the heart. Cardiac output represents a volume of blood that is ejected from the heart over a period of time. For example, the cardiac output may be quantified in terms of the stroke volume (ml/heart beat) times the heart rate (beats/minute). While IEGM signals are a good approximation of cardiac output, IEGM signals are not a direct indicator of hemodynamic performance.
Heretofore, various intra-cardiac indicators (ICI) have been proposed for monitoring cardiac activity, such as heart sounds, blood pressure, and the like. It has also been proposed to monitor certain types of intra-cardiac impedance (within the heart) to derive hemodynamic performance. Intra-cardiac impedance represents impedance that is measured between electrodes that are located within the heart (intra-cardiac electrodes). For example, the intra-cardiac electrodes may be located within the right atrium and the right ventricle with the intra-cardiac impedance measured therebetween. The intra-cardiac electrodes define an intra-cardiac impedance vector that extends through one or both of the atrium and ventricle. The entire intra-cardiac impedance vector or at least a substantially majority of the intra-cardiac impedance vector lies within, and extends through, the blood pool in the chambers of the heart.
Intra-cardiac impedance exhibits a high value when the associated heart chamber(s) are in a systole state. The intra-cardiac impedance exhibits a low value when the associated heart chamber(s) are in a diastole state. As the corresponding heart chambers transition between systole and diastole, the impedance waveform moves between peaks and valleys. The intra-cardiac impedance waveform has not proven to be a good indicator of stroke volume or cardiac output. One limitation of the intra-cardiac impedance waveform arose from the fact that the intra-cardiac impedance vector extends through multiple chambers of the heart. Thus, each measurement of intra-cardiac impedance includes components from individual chambers of the heart, not the overall cooperative effect of all of the heart chambers.
A need remains for an improved method and system for assessing hemodynamic behavior of the heart through an indicator that is direct associated with cardiac output.
Further, not all patients respond equally to implantation of an IMD. The type of IMD, therapy, type and combination of leads and lead placement all impact the effectiveness of the IMD. For example, certain patients who receive pacemakers or CRT devices may respond well, while other patients may not experience a significant improvement in physiologic behavior. During implantation, once the lead(s) are installed the leads are connected to an external pacing system analyzer (PSA). The PSA delivers a desired therapy and the response of the heart is monitored to determine the effectiveness of the lead placement and therapy configuration. The response is measured through IEGM signals or the EKG signals. When a desired response is not achieved, the lead(s) may be replaced or moved, and the timing, voltage and polarity of the therapy may be changed in an effort to improve capture and overall effectiveness. This process is repeated until the IEGM or EKG signals indicate the best result. However, the IEGM and EKG signals are indicators of heart electrical activity, not cardiac output.
A need remains for an improved method and system for assessing and improving cardiac output, during implantation, as well as the overall responsiveness of the patient to the IMD.
Moreover, patients are indicated to receive different types of IMDs based upon various criteria, including the patient's morphology and type of arrhythmia. Depending upon the type of arrhythmia, the patient may be indicated for a pacemaker, a CRT device or a shock only defibrillator. A patient having a low cardiac ejection fraction may receive a CRT device or a shock only defibrillator. When the patient exhibits low ejection fraction (EF) and has a narrow QRS complex (e.g., less than 130 to 140 ms), the patient will not be indicated for a CRT device (e.g. contra-indicated). The contra-indication occurs because cardiac resynchronization therapies have not been shown to have sufficient efficacy for patients with a narrow QRS complex. Thus these patients are not expected to realize a benefit from the CRT therapies available by a CRT device with a CRT lead. Thus, patients with a low EF and narrow QRS complex are indicated for shock only defibrillators and receive a shock only type of lead.
However, certain patients may benefit from CRT therapies even when the patient has a narrow QRS complex. Today, no convenient and cost effective mechanism exists to determine whether a patient, who has a narrow QRS complex, may still benefit from a CRT device. A need exists for a method and system that is capable of assessing intraoperatively, during implantation, whether CRT therapies would improve the cardiac output of an individual, notwithstanding a narrow QRS complex.